Citations 708

Major Adverse Cardiovascular Events in Patients Treated With Anthracyclines for Breast Cancer or Lymphoma: 25-Year Follow-Up

No container title available | June 10, 2025 | Volume: No volume available | Issue: No issue available | Pages: No page available

10.21203/rs.3.rs-6778136/v1

Abstract Background Anthracyclines (ACs) are a risk factor for heart failure (HF), but their impact on broader composite outcomes such as major adverse cardiovascular events (MACE) remain less well characterized. From the Rochester Epidemiology Project, we identified patients with breast cancer or lymphoma to assess for association between AC use and MACE in these patients with > 25 years of follow-up. Methods We identified patients with cancer, with or without an AC as first-line treatment, and a control group of individuals without cancer, matched by age, sex, and cardiovascular comorbid conditions to the cancer patients. Outcomes of interest were 3-MACE (myocardial infarction, stroke, and cardiovascular death), and 4-MACE (3-MACE plus HF). Cox regression analysis was used to identify variables associated with MACE at 5, 10, and 25 years of follow-up. Results Of 812 patients with cancer, 675 had AC treatment (AC group) and 137 did not (no-AC group); the control group comprised 1,384 matched patients without cancer. The risk of 3-MACE was similar among the 3 groups at all time points. Older age, male sex, and hypertension were associated with 3-MACE. The risk of 4-MACE was similar between the control and no-AC groups; the risk was increased for the AC group vs controls at all time points. Older age, male sex, smoking history, type 2 diabetes, and hypertension were associated with 4-MACE. Conclusions Cardiovascular risk factors are the main drivers of 3-MACE and ACs increase the risk of 4-MACE given their association with HF. This underscores the importance of implementing lifestyle changes among these patients.
Assessing the effects of financial toxicity on quality of life among hematopoietic stem cell transplantation recipients.

Journal of Clinical Oncology | May 28, 2025 | Volume: 43 | Issue: 16_suppl | Pages: 1593-1593

10.1200/jco.2025.43.16_suppl.1593

1593 Background: “Financial toxicity” refers to the financial burden imposed by treatment costs on individuals with cancer, constituting a major barrier to achieving equitable cancer outcomes. Recent literature increasingly demonstrates the detrimental impacts of financial toxicity on quality of life (QOL) among individuals with cancer, including individuals who have undergone hematopoietic stem cell transplantation (HSCT). This study evaluates associations among treatment cost burden and various aspects of QOL following HSCT. Methods: Seven hundred one HSCT recipients completed a survey examining their biopsychosocial health one year following transplant. The survey included the Functional Assessment of Cancer Therapy – Bone Marrow Transplantation (FACT-BMT), a multifactorial measure of QOL specific to this population. Treatment cost burden endorsement was measured on a 5-item Likert scale. Hierarchical regression models were developed to assess the incremental effects of demographic characteristics (i.e., Block 1), clinical predictors (Block 2), and cost burden (Block 3) on physical, emotional, social, functional, BMT-specific, general, and composite QOL outcomes. Results: Significant model improvement was observed with the addition of clinical factors ( ΔF(2,650) = 20.28, p < .001), and subsequently, treatment cost burden ( ΔF(1,649) = 110.29, p < .001). In the final model, higher cost burden was associated with poorer physical (β = -0.323, p < .001), emotional (β = -0.301, p < .001), social (β = -0.250, p < .001), functional (β = -0.317, p < .001), BMT-specific (β = -0.341, p < .001), general (β = -0.377, p < .001), and composite QOL (β = -0.381, p < .001). Poorer performance score was associated with each QOL indicator ( p < .001), with allogeneic transplant type associated with poorer functional (β = -0.001, p = .002), but higher emotional (β = 0.118, p = .002), wellbeing. Older age (β = 0.113, p = .003) and female sex predicted higher (β = 0.183, p < .001), while Hispanic ethnicity predicted poorer (β = -0.095, p = .010), social wellbeing. Female sex was associated with poorer QOL specific to BMT concerns (β = -0.118, p = .001). Conclusions: Higher treatment cost burden is associated with poorer overall QOL and its physical, emotional, social, functional, and BMT-specific components one year following HSCT, after controlling for demographic and clinical characteristics. This reflects a critical barrier to equitable cancer care, suggesting that financial toxicity may perpetuate preexisting inequities in QOL, treatment, disease, and survival outcomes that disproportionately impact the underserved. Future research should prioritize 1) better understanding relationships among complex indicators of financial toxicity, QOL, and their underpinning mechanisms and 2) developing solutions to mitigate financial toxicity of HSCT and overall cancer care.
Racial/ethnic disparities in neoplasm mortality and the role of healthcare access in the United States: Insights from the Global Burden of Disease study study 2000–2019.

Journal of Clinical Oncology | May 28, 2025 | Volume: 43 | Issue: 16_suppl | Pages: No page available

10.1200/jco.2025.43.16_suppl.e13738

e13738 Background: Persistent racial/ethnic and regional disparities in neoplasm mortality remain significant public health challenges. This study evaluates long-term trends in neoplasm mortality by race/ethnicity at the county level in the United States and examines the relationship between hospital density and mortality. Methods: Using data from the Global Burden of Disease Study (2000-2019), we analyzed age-standardized mortality rates (ASR) for neoplasms by ethnicity/raceHispanic (all races) and non-Hispanic American Indian or Alaska Native (AIAN), Asian or Pacific Islander (API), Black, and White. A joinpoint regression analysis was used to identify significant changes in the mortality trends, summarized as average annual percent change (AAPC). Correlation analysis evaluated the relationship between county-level hospital density and neoplasm mortality. Results: Neoplasm mortality rates declined across all racial/ethnic groups from 2000 to 2019, but disparities persisted. ASR per 100,000 population decreased from 240.5 (95% UI: 214.3–269.9) to 203.0 (180.8–228.3) for AIAN, 149.5 (144.9–153.9) to 115.3 (111.7–118.7) for API, 314.5 (312.1–317.0) to 218.7 (217.1–220.3) for Black, 168.4 (164.6–172.0) to 133.8 (131.0–136.4) for Latino, and 241.2 (240.5–242.0) to 187.5 (186.9–188.2) for White. AAPC from 2000 to 2019 ranged from -0.94% (AIAN) to -1.90% (Black). Gender-specific analyses revealed similar trends, with males showing slightly greater declines. Southeast states experienced slower declines compared to the Northeast. Some counties exhibited worsening mortality trends, particularly for AIAN, API, and Latino. The county-level hospital density (table) showed weak but statistically significant correlations in 2019 for AIAN (r = -0.35; p < 0.0001), White (r = -0.15; p < 0.0001), and Black (r = -0.18; p < 0.0001). No inverse correlation was observed for API (r = 0.07; p = 0.071) and Latino (r = 0.06; p = 0.012). Conclusions: While significant progress has been made in reducing neoplasm mortality, racial/ethnic and regional disparities persist, and health care access appears to contribute to this at least in part. Future analyses should evaluate mortality by cancer site and also account for broader clinical and public health infrastructure, as well as social determinants of health to better understand and address underlying disparities. The correlation between hospital density and age-standardized mortality rate from neoplasms by race/ethnicity in 2019. Correlation coefficient with mortality and hospital density AIAN API Black Latino White 2019 -0.35(-0.43 – -0.27) 0.069(-0.0058–0.14) -0.18(-0.23 –-0.13) 0.064(0.014–0.11) -0.15(-0.19 – -0.12)
Clinical characteristics and treatment outcomes of hepatosplenic T-cell lymphoma: Mayo Clinic experience.

Journal of Clinical Oncology | May 28, 2025 | Volume: 43 | Issue: 16_suppl | Pages: 7075-7075

10.1200/jco.2025.43.16_suppl.7075

7075 Background: Hepatosplenic T-cell lymphoma (HSTCL) is a rare, aggressive peripheral T-cell lymphoma arising primarily from γδ T-cells. It carries a poor prognosis and resists conventional chemotherapy. Most reports on HSTCL are case-based. This study comprehensively analyzes a large cohort, evaluating treatment strategies and survival outcomes. Methods: This retrospective study included patients (pts) with pathologically confirmed HSTCL diagnosed between 2000-2024, consecutively seen at Mayo Clinic MN. Clinical, pathological, genomic, and treatment-related data were extracted when available. Descriptive statistics were used to summarize baseline characteristics. Time-to-event analyses, including Kaplan-Meier estimates, median overall survival (OS), and survival time estimates were conducted from the date of diagnosis. Results: A total of 20 patients with newly diagnosed HSTCL were included, with a median age of 57 years (range: 35-71). The cohort was predominantly male (70%) and non-Hispanic (93%). Molecular data was available for five patients, revealing abnormalities in STAT5B, MLL3 deletion, TP53, EZH2, TERT, and NF1 E291D . The median follow-up was 27.6 months (m) with a median OS of 17.6 m (95% CI: 11.2 - NA). First-line treatment was anthracycline-based in 68% of pts and non-anthracycline-based in 32%, with higher response rates in the latter group (50% vs.83%). Although non-anthracycline regimens showed a trend toward improved 3-year OS (100% vs. 29%) the difference was not statistically significant (p = 0.16). Achieving a complete response to first-line therapy was also associated with a trend towards a better 3-year OS compared to refractory disease (80% vs. 50%, p = 0.17). Most pts (79%) underwent hematopoietic stem cell transplant (HSCT), primarily allogeneic, with only one receiving autologous HSCT. First-line therapy before HSCT was evenly distributed between anthracycline (55%) and non-anthracycline (45%) regimens. HSCT recipients had significantly higher 3-year OS than non-recipients (83% vs. 33%, p = 0.017). Notably, the patient with a TP53 mutation has remained in remission for over a year post-allogeneic HSCT. Conclusions: HSTCL predominantly affects younger pts, with nearly half dying within a year. Allogeneic HSCT, rarely used in other NHL subtypes, improved survival. Non-anthracycline regimens and achieving CR trended toward better outcomes. Our study, leveraging a sizable cohort, highlights the need for targeted research and novel therapies to improve HSTCL management. Summary of survival outcomes in HSTCL. Characteristics Median OS (y) 3-Year OS (95% CI) 1.48 [0.93- NA] 46% [0.26 - 0.81] Transplant Transplant NA [NA - NA] 83% [0.58 - 1.00] No Transplant 1.02 [0.93 - NA] 33% [0.07 - 1.00] Treatment Anthracycline Based 1.02 [0.36 - NA] 29% [0.11 - 0.73] Non-Anthracycline Based 4.61 [NA- NA] 100% [1.00 - 1.00]
The optimized HLH inflammatory index: A novel prognostic tool for newly diagnosed patients with diffuse large B-cell lymphoma—Discovery and validation.

Journal of Clinical Oncology | May 28, 2025 | Volume: 43 | Issue: 16_suppl | Pages: 7073-7073

10.1200/jco.2025.43.16_suppl.7073

7073 Background: The Optimized HLH Inflammatory (OHI) index (Zoref-Lorenz et al., Blood , 2022), based on serum soluble CD25 (sCD25) and ferritin, is a prognostic tool identifying inflammation in the hemophagocytic lymphohistiocytosis (HLH) spectrum and early mortality risk. Prior studies were retrospective and enriched with HLH-suspected cases. We hypothesized that the OHI index would predict outcomes in unselected diffuse large B-cell lymphoma (DLBCL). Methods: 670 newly diagnosed DLBCL patients from a prospective cohort (2002–2015) were analyzed: 335 for discovery and 335 for validation. Pre-treatment serum sCD25 and ferritin levels were quantified via ELISA, and we evaluated original thresholds (sCD25 ≥ 3,900 U/mL; ferritin ≥ 1,000 ng/mL) and developed DLBCL-optimized thresholds (using receiver operator curves) for predicting 500-day mortality. We also evaluated event-free survival (EFS), EFS at 24 months (EFS24), and overall survival (OS). Results: The median age was 64, and 51% were male. Using original thresholds, 4.2% (n=14) of patients were OHI+, with a 5.6-fold higher risk of 500-day mortality (95% CI 1.6–17; p<0.001). Optimized thresholds identified 23.6% (n=78) as OHI+ with a 9.2-fold higher 500-day mortality risk (95% CI 4.0–24; p<0.001). Optimized OHI+ also had a higher risk of EFS24 failure and inferior EFS and OS (Table). OHI+ patients had higher rates of B symptoms (35% vs. 20%; p=0.027), elevated LDH (76% vs. 34%; p<0.001), worse performance status (ECOG ≥2: 38% vs. 12%; p<0.001), and advanced-stage disease (Stage IV: 57% vs 38%; p<0.001), though IPI scores (3–5) were not significantly different (44% vs 36%; p=0.28). Adjusting for age and IPI, OHI+ independently predicted 500-day mortality (OR=5.0; CI 1.9–13; p=0.001), EFS24 failure (OR=3.2; CI 1.5–6.5; p=0.0018), and inferior long-term EFS (HR=2.2; CI 1.1–4.3; p=0.030) and OS (HR=2.0; CI 1.0–4.0; p=0.040) at a median follow up of 9.8 years in living patients. In validation, optimized OHI predicted 500-day mortality, EFS24 failure, and long-term OS and EFS (Table). Cytokine profiling revealed elevated inflammatory markers in OHI+ patients, including IL1a (p=0.008), CCL2 (p=0.03), CXCL10 (p<0.001), and CXCL9 (p<0.001), reflecting systemic hyperinflammation. Conclusions: The OHI index is a powerful predictor of early and long-term outcomes in DLBCL patients. Optimized thresholds identify a larger OHI+ group, highlighting hyperinflammation’s critical role in poor outcomes. These findings support its use in routine management and clinical trial design for novel therapies. Odds ratios or hazard ratios and p-values for optimized OHI+ and DLBCL prognosis. Outcome Discovery Validation OR for 500-day mortality 9.2; p<0.001 4.0; p=0.002 OR for EFS24 failure 5.2; p <0.001 6.3; p<0.001 HR for OS 2.3; p<0.001 1.8; p=0.006 HR for EFS 2.4; p<0.001 2.5; p<0.001
Impact of cell of origin, gene rearrangements, and frontline treatment on incidence of secondary central nervous system lymphoma in newly diagnosed diffuse large B-cell lymphoma.

Journal of Clinical Oncology | May 28, 2025 | Volume: 43 | Issue: 16_suppl | Pages: 7052-7052

10.1200/jco.2025.43.16_suppl.7052

7052 Background: Secondary central nervous system lymphoma (SCNSL) is a rare but serious complication that occurs in 2-10% of patients (pts) with diffuse large B-cell lymphoma (DLBCL). The CNS-International Prognostic Index (CNS-IPI) is a validated tool used to assess the risk of CNS relapse. However, with advancements in molecular profiling and treatments, the predictors of SCNSL, including the predictive ability of CNS-IPI combined with other molecular markers and treatment regimens, have become uncertain. This study evaluates new prognostic markers for CNS relapse in DLBCL, focusing on cell-of-origin (COO), gene rearrangements, and treatment types. Methods: DLBCL pts enrolled from 2002-2015 in the Mayo Clinic and University of Iowa Lymphoma Molecular Epidemiology Resource were prospectively followed for incidence of CNS relapse. Pts with primary CNS lymphoma or CNS involvement at diagnosis, and pts treated with high-dose methotrexate containing regimens were excluded. COO classification (GCB vs non-GCB) was determined using Hans algorithm and/or NanoString data. Multivariate Cox regression models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for predictors of SCNSL. Survival analysis was performed from time of DLBCL diagnosis using Cox proportional hazards model. Results: Among 1278 newly diagnosed DLBCL pts included (median age: 63 years; 43.6% female), SCNSL occurred in 46 (3.6%) pts. Pts with SCNSL were more likely to have intermediate/high CNS-IPI scores (80.4%) than pts without SCNSL (63.9%, p=0.02). The 3 yr SCNSL incidence was 0.016 (0.008-0.0033) in low CNS-IPI vs 0.043 (0.031-0.0060) in high CNS-IPI. Those with SCNSL were significantly more likely at baseline to have non-GCB COO (56.3% vs. 36.5%, p=0.02), and advanced stage (76.1% vs. 59.9%, p=0.03) compared to those without SCNSL. The incidence of SCNSL was not influenced by MYC, BCL2, or BCL6 rearrangements, nor by treatment with R-CHOP, R-EPOCH, or other immunochemotherapy regimens. MVA showed that intermediate CNS-IPI (HR 2.32, 95% CI 1.09-4.92, p=0.029), high CNS-IPI (HR 3.59, 95% CI 1.49-8.62, p=0.004), and non-GCB COO (HR 2.19, 95% CI 1.08-4.42, p=0.0029) were independently associated with increased SCNSL risk. After a median follow-up of 12 years (IQR 9–15), overall survival (OS) was 52.1% for the cohort, with OS significantly worse for SCNSL pts (17.4% vs. 53.4%, p<0.001). Conclusions: This large cohort with extensive follow-up highlights the role of COO as an additional prognostic factor for SCNSL while reinforcing CNS-IPI’s prognostic value. Non-GCB COO pts had a higher risk of SCNSL even when adjusted by CNS-IPI risk. Despite advancements in management, SCNSL pts continue to have poor outcomes. Strategies to reduce the incidence of CNS relapse in high-risk pts require further investigation. MER CNS relapse hazard ratios (95% CI). Characteristics Hazard Ratio 95% CI P-Value CNS-IPI Group 0-1 Low Ref Ref Ref 2-3 Intermediate 2.32 1.09 - 4.92 0.029 4+ High 3.59 1.49 - 8.62 0.004 Cell of Origin* GCB Ref Ref Ref non-GCB 2.19 1.08 - 4.42 0.029 Double Hit* non-DHL Ref Ref Ref DHL 1.08 0.14 - 8.3 0.941 Not Done/Missing 1.38 0.76 - 2.51 0.297 Double Expressor* Negative Ref Ref Ref Positive 2.36 0.71 - 7.85 0.162 Not Done/Missing 1.91 0.89 - 4.08 0.097 IC Group* R-CHOP R-EPOCH Ref 1.63 Ref 0.71 - 3.74 Ref 0.249 Other IC 1.18 0.57 - 2.46 0.660 Any EN Involvement* No Ref Ref Ref Yes 0.98 0.51 - 1.88 0.946 Albumin Group* >=Normal Ref Ref Ref <Normal 1.70 0.75 - 3.85 0.201 Head & Neck Involvement* No Ref Ref Ref Yes 0.35 0.048 - 2.63 0.310 *Adjusted by CNS-IPI risk group.
Modifiable Risk Factors in Transplant: Lifestyle Advice and Adherence in a Prospective Cohort Study

American Journal of Health Behavior | May 16, 2025 | Volume: 49 | Issue: 2 | Pages: 66-77

10.5993/ajhb.49.2.7

Objectives: Modifiable lifestyle factors are associated with morbidity and mortality in hematopoietic stem cell transplant (HSCT) survivors. The aims of the study were to examine: (a) receipt of provider advice to change behaviors, (b) health behavior change, and (c) how modifiable lifestyle factors might cluster together. Methods: Patients within a large HSCT program completed a survey (N =870) of lifestyle factors at pre-HSCT evaluation. The survey assessed self-reported adherence to American Cancer Society and HSCT guidelines for cancer survivorship in the year prior to a pre-HSCT evaluation. Lifestyle factors of interest were physical activity, fruit and vegetable consumption, tobacco use, alcohol use, and height/weight to calculate Body Mass Index (BMI). Results: Among patients not meeting all five guidelines (98%), 31% received provider advice to change. Between 10% and 42% reported healthy behavior change since diagnosis. Physical activity, fruit and vegetable consumption, and BMI were the most commonly clustered lifestyle behaviors. Conclusions: A considerable proportion of patients did not meet national guidelines for lifestyle factors. Results highlight an immediate opportunity to improve health care delivery and transplant outcomes via pre-HSCT lifestyle screening and implementation of effective health behavior change interventions.
Abstract 2763: Molecular QTL analyses identify functional variants at inherited risk loci in chronic lymphocytic leukemia

Cancer Research | April 22, 2025 | Volume: 85 | Issue: 8_Supplement_1 | Pages: 2763-2763

10.1158/1538-7445.am2025-2763

Abstract Most disease-associated single-nucleotide polymorphisms (SNPs) identified by genome-wide association studies (GWASs) reside in noncoding regions. There is increasing evidence that they play regulatory roles through epigenetic mechanisms by altering local chromatin state, 3D chromatin structure, and looping interactions. We and others have identified 42 CLL risk loci from GWASs. At 12 risk loci located outside of gene promoters, we previously demonstrated that functional SNPs are highly enriched in enhancers and super-enhancers that mostly target BCL2 family genes and transcriptional regulators. However, the study was limited by using only public epigenomic data generated in lymphoblastoid cell lines (LCL) and normal immune related cell types. To gain a better understanding of how the functional SNPs alter local chromatin state and modulate target gene expression in CLL, we generated RNA-seq data (n=588) and transposase-accessible chromatin with sequencing (ATAC-seq) data (n=69) in CLL tumor B cells. We performed molecular quantitative trait loci (QTL) analysis with index and correlated SNPs (R2 0.5) at 41 risk loci (excluding the HLA locus). The analyses identified cis expression QTLs (eQTLs), within 1Mb of genes’ transcription start site, at 25 risk loci and chromatin accessibility QTLs (caQTLs, within peak) at 11 risk loci, with both eQTLs and caQTLs at 8 risk loci. We identified a total of 54 eGenes, for which the expression is affected by nearby SNPs within 1Mb, including 40 novel eGenes at 16 CLL risk loci not previously reported. Notably, based on publicly available chromosome interaction data from CLL, LCL, and normal B cells, for over 70% of the novel eGenes, their promoters showed looping interactions with the regions carrying the eQTLs. Further, 13 SNPs were identified as both caQTL and eQTL, with the associated novel eGenes including CD81 at 11p15.5, IPCEF1 at 6q25.2, as well as CXXC1 and MBD1 at 18q21.1. The result suggests that these SNPs play a role in altering chromatin accessibility contributed to gene expression variation. At 11p15.5 risk locus, SNP rs2651823 (A/G) represents a novel caQTL and eQTL. The alternative G allele is associated with increased chromatin accessibility and CD81 expression. Hi-C data from GM12878 and CD20+ B cells supported interaction between the open chromatin region carrying rs2651823 and CD81 promoter. CD81 facilitates the trafficking of CD19 to the surface of activated B cells, and CD81-null mice showed impaired immune response. In a mouse model, CD81 contributes to tumor progression and metastasis in Lewis lung carcinoma. In summary, our molecular QTL analysis revealed that functional SNPs, located in CLL risk loci, modulate chromatin accessibility and expression of downstream target genes that could impact CLL risk. Citation Format: Huihuang Yan, Zhiquan Wang, Mingma Hoel, Cristine Allmer, Chantal McCabe, Daniel O’Brien, Dennis Robinson, James Cerhan, Sameer Parikh, Esteban Braggio, Susan Slager. Molecular QTL analyses identify functional variants at inherited risk loci in chronic lymphocytic leukemia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 2763.
Abstract 7344: Family history of hematologic malignancy and prognosis across lymphoma subtypes: Novel association with poor outcomes in follicular lymphoma

Cancer Research | April 21, 2025 | Volume: 85 | Issue: 8_Supplement_1 | Pages: 7344-7344

10.1158/1538-7445.am2025-7344

Abstract Family history of hematologic malignancy (FHHM) is an established risk factor for developing lymphoma, but studies examining associations between self-reported FHHM and lymphoma prognosis during the recent treatment era are limited. Utilizing a prospective cohort study, we evaluated associations between FHHM and prognosis for common lymphoma subtypes, including diffuse large B-cell (DLBCL), follicular (FL), marginal zone (MZL), mantle cell (MCL), Hodgkin (HL), and T-cell (TCL) lymphomas. We used the Mayo Clinic component of the Molecular Epidemiology Resource, a prospective cohort study of newly diagnosed lymphoma patients enrolled from 2002 to 2015. Self-reported FHHM (HL, NHL, leukemia, or multiple myeloma) in a first-degree relative was obtained via questionnaire. Primary outcomes were overall survival (OS) and event-free survival (EFS; time from diagnosis to disease progression, initiation of second-line therapy, or all-cause death). Secondary outcomes were failure to achieve 24 months of event-free survival (EFS24; associated with aggressive disease and poor outcomes) and lymphoma-specific survival (LSS; time from diagnosis to death from lymphoma or lymphoma treatment-related complications). We used multivariable Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CI) for the association of FHHM with OS, EFS, and LSS, and logistic regression to estimate odds ratios (ORs) and 95% CI for the association with failure to achieve EFS24. All models were adjusted for sex and a lymphoma subtype specific prognostic index. The cohort consisted of 650 DLBCL, 679 FL, 291 MZL, 178 MCL, 254 HL, and 196 TCL patients. The prevalence of FHHM ranged from 9.7% in TCL to 14% in FL. FHHM was not associated with OS in any subtype, but MCL patients with FHHM showed an inferior EFS (HR=1.70, 95% CI 1.02-2.85; p=0.04). For EFS24, FHHM was associated with failure to achieve EFS24 only in FL (OR=1.57, 95% CI 0.99-2.48; p=0.05). Similarly, FHHM was associated with inferior LSS in FL patients (HR=1.98, 95% CI 1.11-3.53; p=0.02). In a treatment subgroup analysis of FL patients, the FHHM associations with failure to achieve EFS24 (OR=2.48, 95% CI 1.04-5.74; p=0.04) and inferior LSS (HR=2.68, 95% CI 1.09-6.58; p=0.03) strengthened among those treated with frontline immunochemotherapy (IC). In summary, there were no evidence of associations between FHHM and OS across lymphoma subtypes, but MCL patients with FHHM displayed inferior EFS. FL patients with FHHM were more likely to not achieve EFS24 and to ultimately die of their lymphoma or a lymphoma treatment-related complication. This finding was stronger in more aggressive FL requiring frontline IC. This novel finding would suggest that genetic or environmental factors associated with FHHM may underlie pathways that impact disease aggressiveness and early clinical failure in FL. Citation Format: George Cholack, Raphael Mwangi, Thomas M. Habermann, Verena Hinder, Rosalie Griffen, Dennis Robinson, Andrew L. Feldman, Thomas E. Witzig, Stephen M. Ansell, Brian K. Link, Yucai Wang, Carrie A. Thompson, Susan L. Slager, Matthew Maurer, Anne J. Novak, James R. Cerhan. Family history of hematologic malignancy and prognosis across lymphoma subtypes: Novel association with poor outcomes in follicular lymphoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 7344.
Predictors of Transplant Regret: A Case–Control Study Nested Within a Prospective Cohort of HSCT Recipients

Cancer Medicine | April 2, 2025 | Volume: 14 | Issue: 7 | Pages: No page available

10.1002/cam4.70828 | PMID 40166853

ABSTRACTObjectiveTo explore pre–hematopoietic stem cell transplant (HSCT) demographic, disease, and psychological factors predictive of future transplant regret and to determine post‐HSCT variables associated with regret.Patients and MethodsHSCT candidates participated in a prospective cohort study (June 2008–October 2013) examining health behaviors and HSCT outcomes, including completion of standardized surveys at pre‐HSCT (baseline) and 1‐year post‐HSCT. Cases were participants that endorsed regret at 1‐year post‐HSCT follow‐up, and controls were participants without regret at 1 year, matched on age, sex, and transplant type. For cases and controls, pre‐HSCT psychosocial evaluations were abstracted from the electronic health record and coded to determine the Psychosocial Assessment of Candidates for Transplantation score, psychosocial stressors, and mental health diagnoses. The association of selected factors with regret was estimated with odds ratios and 95% confidence intervals from conditional logistic regression models.ResultsAt post‐HSCT, 49 participants of 638 endorsed transplant regret (8%) and formed the case group; 98 controls were matched from remaining participants. Cases and controls were well matched on age (56.6 vs. 57.2 years), sex (both groups 34.7% female), and transplant type (both groups 81.6% autologous). After controlling for the number of hospitalizations and active treatment status, conditional logistic regression revealed that patients who endorsed regret were 3.7 times (95% CI = 1.37–9.69, p = 0.008) more likely to not be in remission compared to controls at 1‐year post‐HSCT.ConclusionMatched case–control analyses revealed that no pre‐HSCT variables collected during the pre‐HSCT evaluation period were predictive of transplant regret, while poorer outcomes at 1‐year after transplant were associated with regret.